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Sökning: WFRF:(Walles Bengt)

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1.
  • Kannisto, P, et al. (författare)
  • Existence and coexistence of peptides in nerves of the mammalian ovary and oviduct demonstrated by immunocytochemistry
  • 1986
  • Ingår i: Histochemistry. - : Springer Science and Business Media LLC. - 0301-5564 .- 1432-119X. ; 86:1, s. 25-34
  • Tidskriftsartikel (refereegranskat)abstract
    • The immunocytochemical distribution of substance P (SP), gastrin releasing peptide (GRP), vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), and neuropeptide Y (NPY) was studied in the ovary and the Fallopian tube (oviduct) of rats, guinea-pigs, cows, pigs and humans. Generally, the nerve supply was better developed in the oviduct than in the ovary. GRP fibers were most scarce in all tissues. Nerves containing SP were particularly numerous in the oviduct of rat and guinea-pig, supplying the muscular wall and blood vessels. VIP and PHI coexisted in dense plexuses of nerves, not only around blood vessels but also in the follicular wall and the interstitial gland of the ovary, as well as within the smooth muscle layers and subepithelially in the oviduct. The general distribution of NPY was similar, but these immunoreactive nerves were even more numerous. Sequential staining for dopamine-beta-hydroxylase and NPY together with results of chemical sympathectomy with 6-hydroxydopamine suggested that NPY was stored in the noradrenergic sympathetic nerves.
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2.
  • Kannisto, Päivi, et al. (författare)
  • Extracellular and intracellular calcium sources mediating contractile responses of smooth muscle in bovine ovarian follicle and ovarian artery
  • 1987
  • Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 144:3, s. 299-308
  • Tidskriftsartikel (refereegranskat)abstract
    • The relative importance of extracellular and intracellular calcium sources mediating smooth muscle contraction in ovarian follicle and ovarian artery was assessed in experiments on the influence of nifedipine, D-600, amrinone, diethylstilbestrol (DES), lanthanum and/or calcium removal on contractions induced by K+ depolarization, by noradrenaline, histamine and acetylcholine. The K+-induced response was biphasic in the ovarian artery but not in the ovarian follicle. The K+-induced contraction in both preparations was greatly inhibited by nifedipine (1 μM), D-600 (10 μM) and lanthanum (2 mM). Although both phases of the responses in the ovarian artery appeared to be completely dependent on extracellular calcium, phase I was significantly more sensitive to nifedipine than phase II. Incubation in calcium-free medium for 15 min almost abolished the K+-induced contraction. Noradrenaline- and histamine-induced contractions of ovarian follicle were essentially unaffected by nifedipine (1 μM) and D-600 (10 μM) whereas the noradrenaline-induced contraction in ovarian artery was inhibited significantly by D-600 (1 and 10 μM) but not nifedipine (1 μM). In calcium-free medium containing EGTA (1 mM) the responses of ovarian follicle to noradrenaline and histamine were reduced by 26 and 22% respectively. When preparations were stimulated with noradrenaline more than one in calcium-free medium, the contraction decreased progressively compared to time-matched controls. The response was 34% of the control after 50 min in calcium-free medium containing EGTA. In the ovarian artery the response obtained (6% of control) was significantly smaller (P < 0.05) than that in the follicle. Amrinone (100 μM) inhibited both noradrenaline- and K+-induced contractions to a similar degree (about 40%) in the follicle wall. The results indicate that agonist-induced responses of ovarian follicle and artery are mediated by the release of calcium from intracellular stores in addition to influx of extracellular calcium. In contrast, the K+-induced contraction seems to be totally dependent on extracellular calcium. The difference in sensitivity to nifedipine of the two phases of the K+ response in ovarian artery strongly suggests the presence of two different types of K+-activated calcium channels in this smooth muscle.
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3.
  • Rydhstrom, Håkan, et al. (författare)
  • No relation between maternal weight gain and stillbirth
  • 1994
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 1600-0412 .- 0001-6349. ; 73:10, s. 779-781
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND. To evaluate the relationship between stillbirth in singleton pregnancy (> or = 28 weeks gestation) and maternal weight (weight gain) from 24 completed weeks. METHODS. All fetal deaths (n = 210) at five delivery units during seven years in southern Sweden were analysed. To each case a control mother was selected, the only matching criteria being parity and place of delivery. Regression analysis was used for comparison of body weight gain in cases and controls. RESULTS. Mothers experiencing stillbirth had a significantly lower mean body weight at 24 weeks gestation than control mothers (63.5 kg vs 67.3 kg; t = 2.4, p < 0.05). No significant difference between cases and controls was found in mean weight gain during pregnancy from 24 completed gestational weeks to delivery, even when the last three measurements before delivery for cases and controls were compared separately. CONCLUSION. There is no difference in body weight gain between mothers with stillbirth and mothers giving birth to a live infant.
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4.
  • Rydhström, Håkan, et al. (författare)
  • Effects of oophorectomy, sympathetic denervation and sex steroids on uterine norepinephrine content and myometrial contractile response to norepinephrine in the guinea pig
  • 1990
  • Ingår i: Neuroendocrinology. - 0028-3835. ; 52:4, s. 332-336
  • Tidskriftsartikel (refereegranskat)abstract
    • Studies were performed in guinea pigs to elucidate alterations in endogenous uterine norepinephrine (NE) levels and changes in the contractile response to exogenous NE following local sympathetic denervation, oophorectomy, or treatment with sex steroids. Both in intact and oophorectomized animals the myometrial NE concentration was reduced after sex steroid treatment (0.5 microgram 17-beta-estradiol, or 0.1 microgram estradiol plus 2 mg progesterone, during 2 weeks), mainly as a result of increased uterine weight. After surgical removal of the hypogastric nerves and section of the suspensory ligaments, a similar response to sex steroids was seen if the animals had previously been oophorectomized. The myometrial contractile activity induced by exogenous NE was measured in vitro. The EC50 values (NE concentration giving 50% of the maximal response) showed a similar pattern of variations after hormonal treatment and oophorectomy as did the concentration of endogenous NE. Thus, exposure to the steroids leading to a reduction of neuronal NE also caused an increased sensitivity of the myometrial smooth musculature to exogenous NE, and in the various experimental groups the two parameters showed a close and significant relationship. The underlying mechanism may induce a denervation supersensitivity to NE induced by exposure to estrogen and progesterone.
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5.
  • Walles, Bengt, et al. (författare)
  • Maternal health care program and markers for late fetal death
  • 1994
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 1600-0412 .- 0001-6349. ; 73:10, s. 773-778
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE. To identify markers for late fetal death, a multicenter study was performed, based on routinely obtained data from maternal health care units. MATERIAL AND METHODS. Prospectively recorded data were obtained from maternal health care units belonging to five delivery units. In all, 233 consecutive cases of singleton pregnancy involving late fetal death (> or = 28 weeks) were identified between 1983 and 1989. As a control for each case, the next consecutive mother giving birth to a live infant at the same delivery unit was selected, the sole matching criterium being parity. RESULTS. After exclusion of pregnancies with lethal malformations or trauma, 205 cases remained for the statistical analysis. Two main subgroups were identified: mothers with placental abruption (n = 44), and pregnancies with no obvious reason for fetal death (n = 101). An increased risk for late fetal death was evident in expectant mothers > or = 40 years (10 vs 1; chi 2 = 7.6, p < 0.01), and in smokers where an association was seen to placental abruption. A significantly increased risk was also seen in women with medical treatment for essential hypertension (8 vs 1; chi 2 = 5.6, p < 0.05). On the other hand, we found no correlation between proteinuria, glucosuria, decreasing symphysis-fundal height, or changes in the Hb, on the one hand, and late fetal demise, on the other. There was no overrepresentation of post dated pregnancy (by ultrasound early in the second trimester) among the cases. Nor did post dated pregnancies (> or = 42 weeks) estimated from first day of last menstrual period (but not post dated by ultrasound) imply a higher rate of fetal death, as has been suggested in previous studies. CONCLUSION. In the present material, there was no sign of systematic error in the evaluation of data routinely obtained from the antenatal clinics and maternity units. Apart from placental abruption in smokers, a high maternal age, and medical treatment for essential hypertension, deviating data were recorded as often among controls as among cases. No correlation was evident between a post date pregnancy and fetal demise. A short symphysis-fundal height was recorded as often among controls as among cases and the even distribution of fetal birthweight in case pregnancies around the standard curve for the normal population is noteworthy.
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